ANTIDYSRHYTHIMC Flashcards
1
Q
Phase 0 of the myocytes
A
rapid depolarization (influx of Na due to opening of fast Na channels)
2
Q
Phase I of the myocytes
A
partial repolarization inward Na current deactivated, outflow of K
3
Q
Phase 2 of the myocytes
A
Plateau (slow inward of Ca2+ balanced by outward K+ current)
4
Q
Phase 3 of the myocytes
A
repolarization (calcium current inactivates, K+ outflow)
5
Q
Phase 4 of the myocytes
A
Resting membrane potential (Na+ efflux and K+ influx via Na+/K+ ATPase pump)
6
Q
Absolute Refractory period
A
Phase 0-2 & early part of 3, time period where the cell can not depolarize agin
7
Q
Cardiac myocytes
A
Fast response
8
Q
Class I agents works on which phase?
A
Works on phase 0
9
Q
Class II and IV works on which phase?
A
Phase 2
10
Q
Class III and I A works
A
Phase 3
11
Q
Phase 2 drugs are classes
A
Acts on Class II and IV
12
Q
Phase 3 drugs are classes
A
Acts on Class III and IA
13
Q
****Cardiac nodal tissue’s (SA & AV node)
depolarization is largely controlled by
A
Ca2+ channel current and are referred to as slow response tissue
14
Q
Phases of action potential of cardiac
pacemaker (nodal) cells
A
Phase 4 spontaneous depolarization to threshold (also called diastolic depolarization or pacemaker potential) – diffusion of K+ out of cell decreases progressively and diffusion of Na+ into cell increases progressively. During the last 1/3rd of phase 4, Ca2+ ions begin to diffuse into the cell • Phase 0 slow depolarization Ca2+ diffuses into the cell and slight Na+ influx • Phase 3 repolarization –K+ diffuses out of the cell • Pacemaker cells are slow response tissue
15
Q
Are the sodium channels the same for the pacemaker nodal cells?
A
NO
16
Q
PACEMAKER OF MUSCLE CELLS
A
SLOW RESPONSE TISSUE WHEN COMPARED TO MYOCYTE CELLS (BECAUSE THEY DON’T CONDUCT ion movements as fast)
17
Q
Cardiac antidysrhythmic drugs produce their pharmacologic effects by:
A
blocking the passage of ions across Na+, K+, and/or Ca2+ ion channels present in the heart
18
Q
Drugs may decrease automaticity (meaning these agents will slow “automatic” rhythms) by altering any of the 4
determinants of the spontaneous pacemaker discharge
A
- Decrease phase 4 depolarization
- Increase threshold potential
- Increase maximum diastolic potential
- Increase action potential duration
19
Q
*****Vaughan-Williams Classification of
Antiarrhythmic Drugs
A
- Class I- Na+ Channel Blockers (fast Na only)
- Class II- Beta-adrenergic Blockers
- Class III - K+ Channel Blockers
- Class IV - Ca2+ Channel Blockers (only VERAPAMIL and DILTIAZEM
20
Q
***Class IA Names
A
– Quinidine (PDQ)
– Procainamide
– Disopyramide
21
Q
**Class II Names
A
Esmolol (MEPA)
Acebutalol,
Propranolol,
Metoprolol
22
Q
*** Class III Names
A
- Amiodarone (ADIDS) – Dronedarone – Dofetilide – Ibutilide – Sotalol
23
Q
***Class IB Names
A
– Lidocaine (LPM)
– Mexiletine
– Phenytoin
24
Q
***Class IC Names
A
– Flecainide (FP)
– Propafenone
25
***Class IV Names
– Verapamil
| – Diltiazem
26
The following agents are also anti-arrhythmic drugs but do
| not fit into the Vaughan-Williams Classification system
Digoxin (DAMI)
– Adenosine
– Magnesium
– Ivabradine (Corlanor)
27
Class I agents are classified as Na+ channel blockers (fast Na+ channels)
• Class I anti-arrhythmic drugs bind to and block/inhibit fast Na+ channels that are responsible for the rapid depolarization (phase 0) in non-nodal tissue, which results in the following:
– Inhibits depolarization by reducing the rate of rise of phase 0 of the action potential, also known as Vmax (aka: Decreases phase 0 of the fast action potential) and decreases the amplitude of the cardiac action potential
– Slows conduction velocity in atria, ventricles and His-Purkinje fibers (non-nodal tissue)
– Decreases automaticity
28
Antidysrhythmic effects are due to blockade of the responses
of beta-adrenergic receptors in the heart to SNS stimulation, as
well as the effects of circulating catecholamines
* Class II drugs are beta-adrenergic antagonists
| * Every beta-blocker on the market is a Class II agent!
29
Class II mechanism of action (NODAL)
Decrease automaticity by decreasing the rate of phase 4 spontaneous depolarization of SA node.
Decrease AV nodal conduction velocity
Negative chronotrophic
Negative Inotrope (decrease phase II of non-nodal tissue
Can produce AV block
30
Class III agents are classified as
K+ channel blockers.
31
Class III antiarrhytmic drugs bind to and blcok
K+ ion channels which prolong repolarization (phase III) by :
prolonging the duration of the cardiac action potential and the effective refractory period (ERP) (prolong refractoriness) of atrial and ventricular myocytes
32
Class IV: Mechanism of action (MYOCYTES)
Verapamil and diltiazem act by inhbiting the influx of Ca2ions acrross slow L-type voltage-gated ca2+ channels of CARDIAR MYOCYTES, SA and AV nodal
So they are NEGATIVE INOTROPE.
NEVER GIVEN TO Heart failure with Decreased EF (HfrEF)
33
Class IV agents increase the (in NODAL)
Threshold voltage resulting in decreased amount of Ca2+ entry into the nodal cell.
Took longer for phase IV to reach
34
**Class IV mechanism of action (NODAL)
Inhibiting calcium entry into the cardiac NODAL tissue cells results in :
1. Decreased rate of spontaneous phase 4 depolarization
2. Decreased SA and AV node automaticity
3. Decreased Conduction velocity through AV node (negative dromotrope)-->Prolonged PR
4. Decrease HR
5. Increased Refractory Period.
35
Class IV agents : effects of only those 2 drugs, but NOT a class IV mechanism
Inhibits calcium entry into vascular smooth muscle tissue which results in relaxation of vascular smooth muscle of coronary arteries and systemic arteries (HYPOTENSION mechanism)
36
Useful in reentrant tachycardia that arise from or use the SA and AV nodes
Verapamil and Diltiazem
37
Class I - Na+ Channel Blockers
| Another difference:
```
All class I agents have a predominant affinity for a particular state of the Na + channels when they block the Na+ channel, which influences its clinical effects
- Affinity during activation and/or inactivation.
```
38
All Class I agents possess a
property called rate dependence (used dependence), their sodium channels are best at fast HR
39
Na+ Channel blockade and slowing of conduction by the drugs is
GREATEST at fast heart rates and least during Bradycardia.
40
Sodium channel blockers work better
when HR is higher.
41
Which category Class IA agents:
All class IA In addition to blocking fast Na+ channels ALSO block K+ channels in the heart.
They have Class I and Class III effects.
Non-nodal tissues
42
```
All class IA agents have proarrythmic agents: By blocking ________they do what? putting patient at risk for _______
Significant ______ _____
```
blocking potassium Channels( prolonged QT ) Increase Torsades de pointes
Significant negative inotropes.
43
Class IA drugs are broad spectrum agentst and are effective for both
SVTs and Vtach
44
****Class ____are rarely used for anesthesia due to ______ ______
Profound HYPOTENSION
45
Quinidine Class IA
```
is a class IA agents that blocks Na+ channels in the "open' state only AND also blocks K+ currents/channels
Posess alpha adrenergic ANTAGONIST, anticholinergic effecfs and ANTIMALARIAL EFFECTS
```
46
Clinical use of Quinidine first slide not important.
Last resorts for Atrial or ventricular arrhythmias
47
Additional pharmacological effects
Prolong QRS and *****QT interval
| Shortened PR
48
Metabolism of Quinidine
metabolize in liver via CYP3A4
active metabolites
HIGHLY PROTEIN BIND to ALBUMIN80-90
20% Kidney as unchanged drug.
49
Avoid quinidine in
HF patients
50
Quinidine SIDE EFFECTS
```
*****Diarrhea (most common)
Nausea
Syncope
HYPOTENSION
REFLEX TACHYCARDIA
```
51
Quinidine Immunological reactions
LUPUS-LIKE REACTIONS
52
Cinchonism with ________include
Quinidine; tinnitus, headache, decreased hearing acuity, blurring vision
53
*****Quinidine -Drug interactions
****Potentiates/ACCENTUATES non-depolarizing and depolarizing neuromuscular blockers.
54
Quinidine increases ______serum concentration.
digoxin
55
Decrease quinidine concentration
CYP 3A4 inducers
56
INcrease quinidine concentration
CYP3A4 inhibitors
57
Quinidine has a ______adrenergic antagonists which can produce _______-
alpha; Vasodilation.
58
PROCAINAMIDE is a ________ and it
Class IA ; blocks Na+ channels in the open state and ALSO blocks K+ current/channels, and has a VERY WEAK anticholinergic effects. Same electrophysiologic
59
Clinical use of Procainamide
Does same as quinidine except does not have ANTAGONISTIC PROPERTIES
60
PROCAINAMIDE Dosing
In urgent situation for VTACH conversion
| 100mg IV every 5 minutes until 15mg/kg given, the arrhythmia ceases OR the QRS widens >50%
61
Procainamide Afib concersion
Gram IV OVER 30 minutes, then 2mg/min
62
Procainamide is eliminated by both
Renal metabolism and
| hepatic metabolism
63
****Acetylation of procainamide produces an
***active metabolite called NAPA (N-Acetyl procainamide)
64
The activity of N-actetyl transferase enzyme is
determined genetically, patients may either have
| -normal activity or reduced activity (slow acetylators) or increased activity (Fast acetylators)
65
Procainamide clearance required_______
required adequate kidney
66
Both procainamie and NAPA are excreted via the kidneys necessating
dosage adjustements in renal failure patietn.
67
NAPA
has class III effects and prolonged the half life.
68
No oral dose of
Procainamide
69
****BIGGEST CONCERN FOR ANESTHESIA as far as procainamide
*****HYPOTENSION
70
Rapid IV administration of procainamide can lead to hypotension which limits
the use of this agents during general anesthesia
– Hypotension is due to direct myocardial depressive effect
– Never give as a rapid IV bolus
71
Procainamide not given in patients with
heart block --> can lead to systole
72
Oral dosage form of procainamide
NO LONGER AVAILABLE in the USA.
73
Increased effect of nondepolarizing and depolarizing
With procainamide
74
Disopyramide (will never give as anesthesia providers)
possess Na+ channel blockade, K+ channel blockade and has very potent ANTICHOLINERGIC effects
75
Most potent class I agents with anticholinergic effects
DISOPYRAMIDE
76
Most serious side effect of DISOPYRAMIDE
Tachycardia
Dry mouth
URINARY RETENTION
77
Class I B Agents
lidocaine
Mexiletine
Phenytoin
78
Class IB agents action
Less potent Na+ Channel blocks (fast sodium channels) compared to Class IA and IC agents, they produce little effect on shortening Vmax and slowing conduction compared to other class I agents.
79
Class IB agents decrease the effective refactroy period
Shortens refractoriness and shorten the action potential duration in normal cardiac ventricular muscle. UNLIKE IA and IC agents.
80
********Class IB agents decrease the effective refractory period
*******Shortens refractoriness and shorten the action potential duration in normal cardiac ventricular muscle. UNLIKE IA and IC agents.
81
Lidocaine is a ______Agents
is a local anesthetist agent and used in the acute IV treatment of ventricular arrhythmias ONLY
82
Lidocaine: Particular useful in suppresing
re-entry arrhythmias ; NOT USEFUL in ATRIAL ARRYTHMIAS
83
In patients with noram CO, hepatic function and hapetic blood flow
giv In patients with normal cardiac output, hepatic function,
and hepatic blood flow, lidocaine 2mg/kg followed by
continuous infusion of 1 to 4 mg/min should provide
therapeutic drug levels
84
Lidocaine causes (advantages over procainamide and quinidine)
FAR LESS HYPOTENSION
| Less cardiovascular adverse effects.
85
LIDOCAINE On heart conduction:
| Can you use for HF patients
Improves AV conduction
• Action potential duration and effective refractory period
is shortened
- yes
86
• Pulseless VT/VF Conversion or VT with a pulse
| If LVEF < 40%
1 -1.5 mg/kg IV bolus; repeat 0.5-0.75 mg/kg q 3-5 minutes (Maximum of 3mg/kg) If LVEF <40% give 0.5-0.75mg/kg
• VT Maintenance
– 1-4 mg/MINUTE via continuous IV infusion
87
* ******* LIDOCAINE METABOLISM
| * ******* on anesthesia.
*****Because of the rapid rate at which lidocaine is metabolized in the liver, any condition that decreases cardiac output or
decrease liver blood flow can decrease lidocaine clearance and increase risk for toxicity
• Anesthesia, acute MI, congestive heart failure, shock or certain surgical procedures can decrease cardiac output and/
or decrease liver blood flow
88
Lidocaine adverse reaction principal reaction
CNS **stimulation symptoms: SEIZURES, NYGSTAGMUS
| When lidocaine is greater than 5 mcg/ml
89
Lidocaine does what on cardiac contractility?
decreases far less than any other antiarrhythmic used
90
Lidocaine toxication can lead to e
HYPOTENSION
| PERIPHERAL VASODILATION.
91
LIDOCAINE Threshold for seizure is decreased with
Arterial hypoxemia
HYPERKALEMIA
ACIDOSIS
emphasizing the importance of monitoring these parameters during continuous IV lidocaine.
92
• Beta-blockers such as propranolol or cimetidine (Not used IV anymore)
– May reduce hepatic blood flow & thus decrease lidocaine
clearance which can increase lidocaine blood levels and the
increase incidence of adverse reactions, including CNS
adverse effects such as seizures
93
****Mexiletine
s an orally active amine analog of lidocaine
– Mexiletine has been structurally modified to reduce
first-pass hepatic metabolism and permit chronic oral
therapy
94
Does everything lidocaine does but is PO
Mexelitine
95
Phenytoin mechanism of action: same as lidocaine
The effects of automaticity and conduction velocity are similar to lidocaine
Slow the rate of recovery of voltage activateted Na+ ions from inactivation
Shortens QT
96
Phenytoin exhibits _______pharmacokinetics which is a type of
Michaelis-Mentin pharmacokinetics,
| which is a type of non-linear pharmacokinetics where phenytoin’s metabolism is saturable
97
Clinical Use of Phenytoin
– Suppression of ventricular dysrhythmias.
– Rarely used anymore, used primarily as an anticonvulsant
Dose______
– Note: will precipitate with D5W; use normal saline only
– Max infusion rate is 50 mg/min, infusing faster than this
can cause profound myocardial depression
• Will be reviewed later in more detail with anticonvulsant
medication
Suppression of ventricular dysrhythmias (VTach and Tdp)
Dose: 100 mg IV q 5 minutes (1.5 mg/kg) or 10 to 15 mg/
kg (1000 mg max) has been given
98
*****Max infusion rate is _____mg/min, infusing faster than this can cause_______
50 mg/min, profound myocardial depression
99
Class IC agents are the most ________
POTENT ARRHYTHMIC AGENTS at slowing CONDUCTION VELOCITY of the cardiac impulse and decreasing the rate of phase 0 depolarization> they dissociate slowly from the Na channels.
100
Class IC agents are ABSOLUTELY CONTRATINDICATED in
patients with structural heart disease (i.e.: previous MI)
due to increased mortality rates in these types of
patients which was based on results of the CAST trial
In
patients with structural heart disease (i.e.: previous MI)
due to increased mortality rates in these types of
patients which was based on results of the CAST trial
101
****PROPAFENONE Class IC
*****– Also has weak beta-blocker properties since it is structurally
similar to beta-blockers
– Also posseses calcium-channel blocking effects
102
******Propafenone is extensively metabolized in the
Metabolized extensively in liver by CYP 450
– Follows nonlinear pharmacokinetics
– Has pharmacologically active metabolites
103
Not given in BRONCHOSPASMS patients.
Non-selective beta blocks
104
A structural analog of thyroid hormone (thyroxine)
Amiodarone is highly lipophilic, is concentrated in many tissues and is eliminated extremely slowly
105
Amiodarone Mechanism of action
– K+ channel blockade (Class III)
– Na+ channel blockade of inactivated state (Class I)
– Non-selective beta-blocking properties (Class II)
– Some Ca2+ channel blockade activity (Class IV)
– Amiodarone possesses electrophysiologic characteristics from all 4
Vaughan Williams classes
– Also blocks alpha-adrenergic receptors
106
******Amiodarone Mechanism of action
– K+ channel blockade (Class III)
– Na+ channel blockade of inactivated state (Class I)
– Non-selective beta-blocking properties (Class II)
– Some Ca2+ channel blockade activity (Class IV)
*****Amiodarone possesses electrophysiologic characteristics from all 4
Vaughan Williams classes
– Also blocks alpha-adrenergic receptors
107
****Amiodarone possesses
Amiodarone possesses electrophysiologic characteristics from all 4
Vaughan Williams classes
108
Although amiodarone prolongs the QT interval, its use is associated with a lower incidence to TdP than Class 1A and other Class III agents
– TdP is the most common arrhythmia seen with amiodarone
use (proarrhythmic agent)
• Dosage adjustments are not required in hepatic, renal or
cardiac dysfunction
PROARRHYTHMIC agent
| Rare Torsades de pointes.
109
Clinical uses for Amiodarone
Used for every known arrrhtymias, above or in ventricles.
110
Onset of action with amiodarone
onset : 8-24 months
| Peak effect: 1 week to 5 months
111
Amiodarone to
Concentrated in many tissues
| HIGH Vd
112
Duration of effect after discontinuation
7-50 days because of LARGE
113
Half life of amiodarone
LONG , nobody know about 40 days
114
AMIODARONE can still be use in
liver failure.
115
Can you dialize amiodarone
No
116
*****The most serious adverse effect during CHRONIC AMIODARONE therapy is
****PULMONARY FIBROSIS, which can be fatal.
117
Screening test such as : 4 tests NEEDED For amiodarone therapy.
CXray
Pulmonary function tests
Thyroid panel
Liver fuction s
118
3 top considerations for amiodarone.
High volume of distribution
long half life
Pulmonary fibrosis
119
***ANESTHESIA considerations for amiodarone
lowest O2 concentration possible during anesthetic delivery to prevent the formation of free O2 radicals.
120
***2 distinct types of presentation of amiodarone pulmonary toxicity
EALRY ONSET PULMONARY TOXICITY
| PULMONARY ALVEOLITIS
121
Amiadarone major cardiac
AV blocks
HYPOTENSION< HYPOTENSION
Prolong QT interval
122
Amiodarone recommended over
PROCAINAMIDE
123
Can be safely administered in HF
Amiodarone.
124
Amiodarone Thyroid toxicity
Contains 2 iodine molecules --> Can inhibits the conversion of T4 to T3 can cause HYPO or HYPERTHYROIDISM
125
Patient on Amiodarone preop
Check thyroid and liver
126
Amiodarone eye effects
Corneal microdeposits.
127
Drug to drug interactions amiodarone
Numerous
| Think about CYP3A4 inducers and inhibitors.
128
Classic CYP3A4 enzymes inhibitors
AMIODARONE
129
AMIODARONE can increase
Digoxin levels by 50-100%
130
AMIODARONE Can increase level of
Procainamide
| Quinidine
131
Amiodarone dosing
VT/VF pulseless arrect ACLS
300mg/20ml D5W or NS IV push
If VF/pulseless VT recurs, consider 2nd dose 150mg Dose IV push/IO
132
VT/ VF maintenance
1mg/min IV infusion x 6 hours then 0.5mg/min x 18 hours
133
Tachycardia other than VT/VF
150mg IV over 10 minutes.
| Maintenance infusion 1mg/min x 6 hours
134
Sotalol is a (Class ___)
• Mechanism of action
– Inhibits the delayed-rectifier (IKr) current and other K+
currents in cardiac muscle tissue. The K+ channel blockade
is seen at higher dose (>160mg)
– Non-selective beta-adrenergic antagonist at low doses
III; Both a nonselective beta-adrenergic antagonists (low doses) and K+ channel blocker
Inhibits the delayed-rectifier (IKr) current and other K+
currents in cardiac muscle tissue. The K+ channel blockade
is seen at higher dose (>160mg)
135
Use of Sotalol
• Clinical uses
– Sustained VTach or Vfib
– Maintenance of NSR in symptomatic atrial fib/flutter
• Only available as an oral dosage formulation
136
Sotalol is Supplied as a ______mixture both the I and D are equipotent as
Racemic; K+ channel blockers
137
L-enantiomer has more
potent beta adrenergic antagonist
| than the d-enantimorer.
138
Pharmacologic effect SOTALOL
Prolongs the action potential duration (Phase III)
– Prolongs AV refractoriness and action potential duration
– Decreases automaticity
– Slows AV Nodal conduction
– Prolongs the QT interval
– Negative inotrope/chronotrope/dromotrope
139
Sotalol half life is
12 hours.
140
Contraindications of SOTALOL
Bronchial asthma, left venticular dystrophy, prolong QT intervals, 2nd and 3rd degree AV blocks
Tordades
HYPOTENSION< BRADYCARDIA
141
Ibutilide
inhibits the IKr in cardiac muscle
delayed repolarization
SLOW SODIUM CHANNELS>
142
Ibutilide: Use for the conversion of
Conversion of recent onset of atrial fibrillilation
143
All class III agents can cause
****TORSADES or other ARRHYTHMIAS
144
Do not study for IBUTILIDE
DOSING.
145
Dofetilide (Tikosyn) is a : CLASS ____agents
Pure K+ channel blocker AVAILABLE only in oral dosage form; III prolongs action potential and prolong repolarization
146
Dofetilide mechanism of action
Blockade of the cardiac ion channel carrying the rapid component of the delayed rectifier potassium current Ikr ****(a pure Ikr blocker) Delayed rectifier
147
Dofetilide Indication (2) : ONLY____
1.Conversion of recent onset atrial fibrillation and atrial flutter to NSR
2.Maintenance of NSR for the recently cardioverted patient.
ATRIAL
148
Dofetilide can prolong
QT Interval
149
Hospitalization and ______ for a minimum of ____hours
ECG monitoring , 72
150
What must be closely monitored: dofetilide.
Renal function and QTc
151
Adverse effected of Dofetilide rare
Headache
chest pain
Dizziness
152
Warning of Dofetilide
Can cause torsades
| Maintain normla potassium
153
Halothane and Dofetilide
Increased risk of cardiac arrhythmia
154
Dofetilide other drugs can prolong QT interval
Phenotiazines,
Haloperidol
Droperinol
Dolasetron.
155
For Dofetilide any drugs that inhibits _______could _______plasma concentration.
inhibis CYP3A5 could increased plasma concentration s of dofetilide
156
Any drug that inhibits Renal secretion of dofetilide will _______Plasma concentration
Increased Acute tubular secretion process
157
Drug to Drugs interaction: Dofetilide
Hypokalemia and HYPOMAGNESEMIA , increasing potential for tornadoes
158
Dronedarone (multaq) is a __________ anti arrhythmic agent that is related to _______and is a _____agent
non-iodinated (NO IODINE) anti arrhythmic agent that is structurally related to amiodarone and is a CLASS III AGENT
159
Mechanism of action of dronedareon
exhibits properties of all 4 classes of Vaughan william classification
MAIN ANTIARRHYTMI: Potassium channel blockade
160
Metabolism
CYP 3A4
161
Side effects of dronedarone
GI issues
162
ANESTHESIA
You can't use any drug prolonging QT interval
163
***Dronedarone contraindicated concomitant use of
Phenothiazines
| Any drug that PROLONGS QT INTERVALS
164
*****No longer use of DRONEDARONE because
Increase risk of death, stroke and HF in decompensated HF or permanent afib
165
MISCELLANEOUS AGENTS
Do not fall into the Vaughan William classification.
166
Adenosine is an ______
Endogenous purine NUCLEOSIDE in all cells of the body with transient NEGATIVE CHRONOTROPIC and DROMOTROPIC EFFECS on cardiac pacemaker tissues
167
****CLINICAL USE OF ADENOSINE
- Paroxysmal SVT (CONVERSION)
| - Not use if they have AFIB
168
****Mechanism of action Adenosine
binds to adenosine recepotr
G-protein coupled receptor
Adenosine 1 receptor in SA node and AV node
Activate receptors ACH sensitive K channels that increase activation of outward K+ current leading to hyper polarization of the cell membrane and shortening got action potential duration. I’m
169
****Mechanism of action
Increases AV node refractoriness via decreased cAMP and decreasing cAMP induced calcium conductance in slow response tissue (AV node)
170
As a result of the mechanism of adenosine:
Slows conduction of cardiac impulses through the AV node (negative dromotrope) and increases AV nodal refractoriness
Slows sinus rate (negative chronotrope)
171
Pharmacokinetisc of Adenosine
1. IV
2. T 1/2 < 10 seconds
3. Rapidly cleared from the circulation through CELLULAR UPTAKE MECHANISM primarily ERYTHROCYTES and vascular endothelial cells.
172
Would hepatic and renal failure expected to alter effectiveness of Adenosine
NO
173
Dosing of Adenosine: Dosing and how many minutes apart.
6mg IV
12 mg IVP x 2 (3 minutes apart)
Max 30 mg
174
Adverse effects of Adenosine
Chest burning tightens due to bronchospasm.
175
***Drugs to drug interactions : Adenosine.
METHYLXANTHINE: Theophylline or caffeine are adenosine antagonist. May required a higher dose of adenosine for effectiveness
176
Dipyridamole does what ?
(adenosine uptake inhibitor)
Increases effect of adenosine
Blocks cellular uptake mechanism of adenosine.
177
Contraindication of adenosine
2nd or 3rd degree HB
178
Ivrabradine (coplanar)
oral agent only , HYPERPOLARIZATION ACTIVATED CYCLIC NUCLEOTDIE GATED CHANNEL BLOCKERS
To control HR and keep it down
179
Ivrabradine (coplanar) mechanism of action
Slow diastolic depolarization by selectively and specifically inhibiting the If current (funny current) which is responsible for regulating the intrinsic pacementer activity in the SA node, this leads to decreased HR
180
Most common adverse effects: Ivrabradine (coplanar)
Brady cardia
| Afib
181
Avoid using with Ivrabradine (coplanar)
verapamil and diltiazem
| will inhibit metabolism of ivabradine. thereby increasing risk of adverse effects such as BRADYCARDIA
